ArticleProceedings of the National Academy of Sciences of the United States of America1999
The Opitz syndrome gene product, MID1, associates with microtubules.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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47 citing papers in PubMed, 137 citations in OpenAlex.
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- Age and Sex-Related Changes to Gene Expression in the Mouse Spinal Cord.Journal of molecular neuroscience : MN · 2019Article
- Novel mTORC1 Mechanism Suggests Therapeutic Targets for COMPopathies.The American journal of pathology · 2019Article
- Age-specific changes in genome-wide methylation enrich for Foxa2 and estrogen receptor alpha binding sites.PloS one · 2018Article
- Two Novel PathogenicMolecular syndromology · 2017Article
- Hedgehog-dependent E3-ligase Midline1 regulates ubiquitin-mediated proteasomal degradation of Pax6 during visual system development.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Mid1/Mid2 expression in craniofacial development and a literature review of X-linked opitz syndrome.Molecular genetics & genomic medicine · 2016Article
- Differential Gene Expression in Liver, Gill, and Olfactory Rosettes of Coho Salmon (Oncorhynchus kisutch) After Acclimation to Salinity.Marine biotechnology (New York, N.Y.) · 2015Article
- Mutations in SPECC1L, encoding sperm antigen with calponin homology and coiled-coil domains 1-like, are found in some cases of autosomal dominant Opitz G/BBB syndrome.Journal of medical genetics · 2015Article
- Midline 1 controls polarization and migration of murine cytotoxic T cells.Immunity, inflammation and disease · 2014Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Opitz syndrome (OS) is a genetically heterogeneous disorder characterized by defects of the ventral midline, including hypertelorism, cleft lip and palate, heart defects, and mental retardation. We recently identified the gene responsible for X-linked OS. The ubiquitously expressed gene product, MID1, is a member of the RING finger family. These proteins are characterized by an N-terminal tripartite protein-protein interaction domain and a conserved C terminus of unknown function. Unlike other RING finger proteins for which diverse cellular functions have been proposed, the function of MID1 is as yet undefined. By using the green fluorescent protein as a tag, we show here that MID1 is a microtubule-associated protein that influences microtubule dynamics in MID1-overexpressing cells. We confirm this observation by demonstrating a colocalization of MID1 and tubulin in subcellular fractions and the association of endogenous MID1 with microtubules after in vitro assembly. Furthermore, overexpressed MID1 proteins harboring mutations described in OS patients lack the capability to associate with microtubules, forming cytoplasmic clumps instead. These data give an idea of the possible molecular pathomechanism underlying the OS phenotype.
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